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WHO IS AN AUTHOR?
815 WHO IS AN AUTHOR?
CHOLECYSTOKININ AND CYSTIC FIBROSIS
SIR,-No less than 54 individual authors wrote the first four papers in your issue of Sept 1, contributing, I calculate, under 200 words of text each. Osler (among others) has stressed that it was the duty of a doctor to do research, but did he mean us thus to cultivate other men’s flowers? I am trying to restrict authorship to a
SiR,-The search for the primary expressed protein defect in cystic fibrosis (CF) continues to be elusive, and has left the medical
maximum of five per paper. Would you be prepared to do the same? MARTIN C. O. BAX, Spastics International Medical Publications,
Senior editor,
5A Netherhall Gardens, London NW3 5RN
Developmental Medicine and Child Neurology
**The multiple authorship Dr Bax mentions raised some eyebrows too. The question "who is an author?"l is asked whenever editors gather, but it is best answered before the typist begins upon the paper. For the truly collaborative study, crossing specialty here
boundaries and
even
oceans,
a
fixed maximum of five could well be
unjust.-ED. L. 1. Editorial. Author! Lancet
1982; ii: 1199.
CENTRAL VEIN CATHETERISATION
SIR,-The combined catheter and cannula for central vein cannulation described by Dr Allison and his colleagues (Aug 18, p 378) is a useful addition to the range of cannulae available. However, the 51% (27 out of 53) success rate in securing immediate access suggests that an alternative route to the central circulation would be welcome. The direct instillation of non-irritant drugs into the bronchial tree via the endotracheal tube is a frequently overlooked route of administration. Absorption is very rapid, approaching that of
intravenous administration. Atropine, adrenaline, isoprenaline, and lignocaine can all be safely administered in a dose 1’ 5-2 times the usual intravenous dose dissolved in 10 ml of sterile water. Irritant drugs such as sodium bicarbonate and calcium salts must be
given intravenously. Repeated frantic attempts at central vein cannulation not only waste time but also frequently result in pneumothorax. Intratracheal instillation is a safe alternative for many of the drugs required during a cardiac arrest and should be considered when venous cannulation is initially unsuccessful. Department of Anaesthesia, University of Leicester, General Hospital, Leicester LE5 4PW 1. Safar P.
Cardiopulmonary cerebral resuscitation. Anaesthesiologists. Stavanger: Laerdal, 1981.
C. D. HANNING World Federation of Societies of
SIR,-While I wholeheartedly agree with Dr Allison and colleagues that central vein catheterisation is mandatory in patients with cardiopulmonary arrest, not only to establish venous access but also to measure central venous pressure, I was surprised that they recommend the infraclavicular subclavian route. The successful catheterisation of 77% of patients implies that access was not successful in 23%-a figure that does not seem to compare favourably with the 17% that Allison et al cite from other sources. Internal jugular catheterisation with the Vygon ’Intraflon’ cannula introduced by a neck approach via the anterior border of the sternomastoid is easy, quick, and safe, without the significant risk of pneumothorax associated with subclavian puncture. This technique should be standard in any patient with cardiopulmonary arrest from any cause, including trauma. Moreover it can be done without the specific attention to the positioning of the patient that is required for safe infraclavicular subclavian catheterisation. Allison et al claim that an advantage of their system is that incompatible drugs (eg, calcium chloride and sodium bicarbonate) can be given via two separate routes. In a patient with circulatory arrest it would surely be more advisable to deliver any such agent acting directly on the myocardium by the most direct route, via an intracardiac needle. Department of General Surgery, Royal Infirmary,
Glasgow G4 0SF
G. H. WELCH
literature awash with conflicting results and speculations. It is thus than usually important that reports of apparent pathological and biochemical abnormalities in this disorder specify with care the material from which observations are drawn. In this respect the claim by Dr Christine and Dr John Gosden (Sept 9, p 541) that a deficiency in the proteolysis of cholecystokinin may be the basic defect in CF is misleading. Their evidence comes from electron micrographs and a table of histological findings on "two fetuses with CF, two with trisomy 13, and one with trisomy 18". Unfortunately, there are considerable doubts about the diagnosis in four of these five cases. The "two fetuses with CF" were the result of termination of pregnancy, occasioned by the finding, in my laboratory, of depressed levels of microvillous enzymes in amniotic fluid supernatant.l,22 This form of prenatal diagnosis is in the early development stage, and there are no firm data on false-positive or false-negative rates. One of these two fetuses may well have had CF (all amniotic fluid microvillous enzymes were abnormal), but doubt remains about the other, in which the y-glutamyltranspeptidase activity was normal. The Gosdens state that the "same termination methods and conditions" were used; however, one pregnancy was terminated by hysterotomy and the other by extra-amniotic prostaglandin infusion. This makes comparisons of post-mortem tissue difficult. Neither fetus had overt meconium ileus, an observation claimed by Muller et al3 to be the most obvious sign of fetal CF. Furthermore, the Gosdens do not report that one of the two cases of trisomy 13 and the single case of trisomy 18 were part of the same prospective series of prenatal diagnoses on patients with a 1-in-4 risk of CF. In both cases amniotic fluid alkaline phosphatase assay pointed to CF. The fact that a chromosomal abnormality was subsequently discovered, thus leading to termination of pregnancy, does not exclude the possibility that one both also had CF. In a paper with Christine Gosden and others4 we pointed out that only 21% (3 in 14) of amniotic fluids from trisomy 18 pregnancies had abnormal alkaline phosphatase activities. So far I have examined four amniotic fluids from cases of trisomy 13 and in only the single case, also at risk for CF, were microvillous enzyme activities abnormal. Thus these two control fetuses are not typical examples of trisomy 13 and trisomy 18, and have some indications of CF. Much of the confusion and lack of reproducibility in publications on CF may arise from inadequate reporting. The Gosdens should have included the above vital information. By not doing so they do a disservice to others who have laboured long and fruitlessly on this baffling disease. more
or
Human Genetics
Unit,
University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU 1. 2.
DAVID J. H. BROCK
Brock DJH. Amniotic fluid alkaline phosphatase isoenzymes in early prenatal diagnosis of cystic fibrosis. Lancet 1983; ii: 941-43. Brock DJH, Bedgood D, Hayward C. Prenatal diagnosis of cystic fibrosis by assay of
fluid microvillar enzymes. Hum Genet 1984; 65: 248-51. F, Frot JC, Aubry MC, Boué J, Boué A. Meconium ileus in cystic fibrosis fetuses. Lancet 1984; ii: 223. 4. Brock DJH, Bedgood D, Hayward C, Carbarns NJ, Gosden C. Amniotic fluid amniotic
3. Muller
microvillar enzyme activities in the
early detection of
fetal abnormalities. Prenatal
Diagnosis 1984; 4: 261-66.
***We
showed this letter
whose
reply follows.-ED.L.
to
Dr Christine and Dr
John Gosden,
SiR,-Dr Brock criticises us for claiming that deficiency of an enzyme involved in CCK proteolysis may be the basic defect in CF. We made no "claim", but suggested this simply as a hypothesis which is consistent with our observations in fetuses and accords with the features of individuals with CF, and is susceptible to further testing. The essential basis of the ultrastructural and histochemical microvillar enzyme studies was that the abnormal fetuses were compared with 15 normal controls. It is stated explicitly in the text that different methods of termination were used, and that it was the
CHOLECYSTOKININ AND CYSTIC FIBROSIS
SIR,-No less than 54 individual authors wrote the first four papers in your issue of Sept 1, contributing, I calculate, under 200 words of text each. Osler (among others) has stressed that it was the duty of a doctor to do research, but did he mean us thus to cultivate other men’s flowers? I am trying to restrict authorship to a
SiR,-The search for the primary expressed protein defect in cystic fibrosis (CF) continues to be elusive, and has left the medical
maximum of five per paper. Would you be prepared to do the same? MARTIN C. O. BAX, Spastics International Medical Publications,
Senior editor,
5A Netherhall Gardens, London NW3 5RN
Developmental Medicine and Child Neurology
**The multiple authorship Dr Bax mentions raised some eyebrows too. The question "who is an author?"l is asked whenever editors gather, but it is best answered before the typist begins upon the paper. For the truly collaborative study, crossing specialty here
boundaries and
even
oceans,
a
fixed maximum of five could well be
unjust.-ED. L. 1. Editorial. Author! Lancet
1982; ii: 1199.
CENTRAL VEIN CATHETERISATION
SIR,-The combined catheter and cannula for central vein cannulation described by Dr Allison and his colleagues (Aug 18, p 378) is a useful addition to the range of cannulae available. However, the 51% (27 out of 53) success rate in securing immediate access suggests that an alternative route to the central circulation would be welcome. The direct instillation of non-irritant drugs into the bronchial tree via the endotracheal tube is a frequently overlooked route of administration. Absorption is very rapid, approaching that of
intravenous administration. Atropine, adrenaline, isoprenaline, and lignocaine can all be safely administered in a dose 1’ 5-2 times the usual intravenous dose dissolved in 10 ml of sterile water. Irritant drugs such as sodium bicarbonate and calcium salts must be
given intravenously. Repeated frantic attempts at central vein cannulation not only waste time but also frequently result in pneumothorax. Intratracheal instillation is a safe alternative for many of the drugs required during a cardiac arrest and should be considered when venous cannulation is initially unsuccessful. Department of Anaesthesia, University of Leicester, General Hospital, Leicester LE5 4PW 1. Safar P.
Cardiopulmonary cerebral resuscitation. Anaesthesiologists. Stavanger: Laerdal, 1981.
C. D. HANNING World Federation of Societies of
SIR,-While I wholeheartedly agree with Dr Allison and colleagues that central vein catheterisation is mandatory in patients with cardiopulmonary arrest, not only to establish venous access but also to measure central venous pressure, I was surprised that they recommend the infraclavicular subclavian route. The successful catheterisation of 77% of patients implies that access was not successful in 23%-a figure that does not seem to compare favourably with the 17% that Allison et al cite from other sources. Internal jugular catheterisation with the Vygon ’Intraflon’ cannula introduced by a neck approach via the anterior border of the sternomastoid is easy, quick, and safe, without the significant risk of pneumothorax associated with subclavian puncture. This technique should be standard in any patient with cardiopulmonary arrest from any cause, including trauma. Moreover it can be done without the specific attention to the positioning of the patient that is required for safe infraclavicular subclavian catheterisation. Allison et al claim that an advantage of their system is that incompatible drugs (eg, calcium chloride and sodium bicarbonate) can be given via two separate routes. In a patient with circulatory arrest it would surely be more advisable to deliver any such agent acting directly on the myocardium by the most direct route, via an intracardiac needle. Department of General Surgery, Royal Infirmary,
Glasgow G4 0SF
G. H. WELCH
literature awash with conflicting results and speculations. It is thus than usually important that reports of apparent pathological and biochemical abnormalities in this disorder specify with care the material from which observations are drawn. In this respect the claim by Dr Christine and Dr John Gosden (Sept 9, p 541) that a deficiency in the proteolysis of cholecystokinin may be the basic defect in CF is misleading. Their evidence comes from electron micrographs and a table of histological findings on "two fetuses with CF, two with trisomy 13, and one with trisomy 18". Unfortunately, there are considerable doubts about the diagnosis in four of these five cases. The "two fetuses with CF" were the result of termination of pregnancy, occasioned by the finding, in my laboratory, of depressed levels of microvillous enzymes in amniotic fluid supernatant.l,22 This form of prenatal diagnosis is in the early development stage, and there are no firm data on false-positive or false-negative rates. One of these two fetuses may well have had CF (all amniotic fluid microvillous enzymes were abnormal), but doubt remains about the other, in which the y-glutamyltranspeptidase activity was normal. The Gosdens state that the "same termination methods and conditions" were used; however, one pregnancy was terminated by hysterotomy and the other by extra-amniotic prostaglandin infusion. This makes comparisons of post-mortem tissue difficult. Neither fetus had overt meconium ileus, an observation claimed by Muller et al3 to be the most obvious sign of fetal CF. Furthermore, the Gosdens do not report that one of the two cases of trisomy 13 and the single case of trisomy 18 were part of the same prospective series of prenatal diagnoses on patients with a 1-in-4 risk of CF. In both cases amniotic fluid alkaline phosphatase assay pointed to CF. The fact that a chromosomal abnormality was subsequently discovered, thus leading to termination of pregnancy, does not exclude the possibility that one both also had CF. In a paper with Christine Gosden and others4 we pointed out that only 21% (3 in 14) of amniotic fluids from trisomy 18 pregnancies had abnormal alkaline phosphatase activities. So far I have examined four amniotic fluids from cases of trisomy 13 and in only the single case, also at risk for CF, were microvillous enzyme activities abnormal. Thus these two control fetuses are not typical examples of trisomy 13 and trisomy 18, and have some indications of CF. Much of the confusion and lack of reproducibility in publications on CF may arise from inadequate reporting. The Gosdens should have included the above vital information. By not doing so they do a disservice to others who have laboured long and fruitlessly on this baffling disease. more
or
Human Genetics
Unit,
University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU 1. 2.
DAVID J. H. BROCK
Brock DJH. Amniotic fluid alkaline phosphatase isoenzymes in early prenatal diagnosis of cystic fibrosis. Lancet 1983; ii: 941-43. Brock DJH, Bedgood D, Hayward C. Prenatal diagnosis of cystic fibrosis by assay of
fluid microvillar enzymes. Hum Genet 1984; 65: 248-51. F, Frot JC, Aubry MC, Boué J, Boué A. Meconium ileus in cystic fibrosis fetuses. Lancet 1984; ii: 223. 4. Brock DJH, Bedgood D, Hayward C, Carbarns NJ, Gosden C. Amniotic fluid amniotic
3. Muller
microvillar enzyme activities in the
early detection of
fetal abnormalities. Prenatal
Diagnosis 1984; 4: 261-66.
***We
showed this letter
whose
reply follows.-ED.L.
to
Dr Christine and Dr
John Gosden,
SiR,-Dr Brock criticises us for claiming that deficiency of an enzyme involved in CCK proteolysis may be the basic defect in CF. We made no "claim", but suggested this simply as a hypothesis which is consistent with our observations in fetuses and accords with the features of individuals with CF, and is susceptible to further testing. The essential basis of the ultrastructural and histochemical microvillar enzyme studies was that the abnormal fetuses were compared with 15 normal controls. It is stated explicitly in the text that different methods of termination were used, and that it was the